Last year the local anesthetic lidocaine (but not other local anesthetics: cocaine, procaine or tetracaine) was found to bind with high affinity (k D=355 nM) to peripheral-type benzodiazepine (BZ) receptors (PBR) in rat olfactory bulb membranes, suggesting that the anticonvulsant or convulsant effects of lidocaine may involve a PBR component. This possibility was further investigated under another BPB project (Z01MH 02526-02 BP). Studies on the regulation of central adenosine and beta-adrenergic receptors by alterations in thyroid functions in rats were started last year. However, Dr. Stein (the major contributor to that work) has moved to the University of Manitoba where he is continuing this project in collaboration with us. This investigation is still in the initial stages and the data require further analysis before any conclusions can be made. Studies on identifying the hypothesized central adenosine A3 receptor (begun last year) have led to the discovery of an endogenous ADP- ribosylation caused by a compound that was found to differentially alter agonist binding to adenosine A1 and A2 receptors. The compound is herein referred to as CX. CX stimulated adenosine A1 binding modestly (up to 20% at 1 mM) while it dose-dependently inhibited adenosine A2 binding (up to 42% at 1 mM). Moreover, CX dose-dependently inhibited PBR binding almost completely but had no effect on binding at the central-type BZ receptor. The effect of CX on PBR binding was potentiated by MgCl2. It was found that CX dose-dependently stimulated the breakdown of nicotinamide adenine dinucleotide with the subsequent incorporation of the breakdown product ADP-ribose into the brain proteins (ADP-ribosylation). This effect of CX is markedly potentiated by MgCl2.